The overall objective of the poposed research is to test the hypothesis that the renal nerves represent an important afferent and efferent control system for the regulation of several renal functions in normal and pathological conditions. Our previous work has identified increased efferent renal sympathetic nerve activity as an important final common pathway mediating the increased renal-sodium retention of edema forming states. The specific aims are: (1) to measure the relative contribution of cardiopulmonary versus sinoaortic baroreceptors to the increase in efferent renal sympathetic nerve activity and renal sodium retention in rats with experimental congestive heart failure due to myocardial infarction, (2) to measure the relative contribution of cardiopulmonary and sinoaortic versus intrahepatic baroreceptors to the increase in efferent renal sympathetic nerve activity and renal sodium retention in rats with experimental biliary cirrhosis due to common bile duct ligation, (3) to measure the relative contribution of cardiopulmonary and sinoaortic baroreceptors versus renal sensory receptors to the increase in efferent renal sympathetic nerve activity and renal sodium retention in rats with experimental nephrotic syndrome due to adriamycin administration. The various experimental models of renal sodium retention and edema formation are well characterized and established in the laboratory. For specific aims 1-3, hemodynamic measurements and electrophysiological techniques (single fiber afferent and efferent nerve fiber recording) will be used to measure the contribution of various putative reflex stations to the increase in efferent renal sympathetic nerve activity and renal sodium retention observed in the models. These studies will serve to more clearly define the pathophysiological alterations in reflex control of efferent renal sympathetic nerve activity in these clinically relevant models of renal sodium retention and edema formation.